(“Introduction to ANS Pharmacology” and “Pharmacology of the ANS - Cholinomimetics & Anticholinergics / Adrenomimetics & Anti-

Adrenergics”).

1. The mechanism of action of reserpine involves:

A. Competitive blockade of postsynaptic alpha-1 adrenoceptors.
B. Inhibition of tyrosine hydroxylase, reducing catecholamine synthesis.
C. Inhibition of the vesicular monoamine transporter (VMAT), leading to depletion of catecholamine stores.
D. Blockade of neuronal reuptake of norepinephrine via NET.
Answer: C) Explanation:

Correct ©: Reserpine irreversibly inhibits VMAT (Vesicular Monoamine Transporter), which is responsible for transporting
monoamines (like
norepinephrine, dopamine, serotonin) from the cytoplasm into synaptic vesicles for storage. By blocking VMAT, reserpine
prevents vesicular storage, leaving the monoamines in the cytoplasm where they are degraded by MAO. This leads to a
profound and long-lasting depletion of neurotransmitter stores in nerve terminals. (ANS Intro Slide 59, 61, 70)
Incorrect (A): This describes alpha-1 blockers like prazosin. Incorrect (B): This describes metyrosine.
(ANS Intro Slide 58)
Incorrect (D): This describes drugs like cocaine and tricyclic antidepressants. (ANS Intro Slide 62)

2. A drug that selectively activates presynaptic alpha-2 adrenoceptors on sympathetic nerve terminals would be expected to cause which of the
following effects?
A. Increased release of norepinephrine from the nerve terminal.
B. Vasoconstriction via direct action on vascular smooth muscle alpha-2 receptors.
C. Decreased release of norepinephrine from the nerve terminal.
D. Increased heart rate via stimulation of cardiac beta-1 receptors.
Answer: C) Explanation:

Correct ©: Presynaptic alpha-2 adrenoceptors on sympathetic nerve terminals

function as autoreceptors. When activated (e.g., by an alpha-2 agonist like clonidine, or by released norepinephrine itself), they
inhibit further norepinephrine release
from that terminal through a negative feedback mechanism. (ANS Intro Slide 49, 85) Incorrect (A): Activation inhibits release, not
increases it.
Incorrect (B): While some postsynaptic alpha-2 receptors can cause vasoconstriction, the question specifies presynaptic alpha-2
activation, which primarily modulates release.
Incorrect (D): This describes beta-1 agonism, not alpha-2 agonism.

3. Which of the following cholinomimetic agents is a quaternary ammonium compound that is poorly absorbed orally and primarily used for its
effects on the gastrointestinal tract and urinary bladder?
A. Pilocarpine
B. Physostigmine
C. Bethanechol
D. Donepezil Answer: C) Explanation:
Correct ©: Bethanechol is a choline ester, a quaternary ammonium compound.
Quaternary amines are poorly lipid-soluble and therefore poorly absorbed from the GI tract and do not readily cross the blood-
brain barrier. Bethanechol is relatively resistant to hydrolysis by cholinesterases and acts selectively on muscarinic receptors,
particularly on smooth muscle of the bladder and GI tract, making it
useful for non-obstructive urinary retention and postoperative ileus. (Cholinomimetics Slide 105, 106)
Incorrect (A): Pilocarpine is a tertiary amine alkaloid, better absorbed and can have systemic effects.
Incorrect (B): Physostigmine is a tertiary amine alkaloid, crosses the BBB. Incorrect (D): Donepezil is designed to cross the
BBB for Alzheimer’s treatment.

4. The primary mechanism by which indirect-acting sympathomimetic amines like amphetamine and tyramine produce their effects is:
A. Direct stimulation of postsynaptic alpha and beta adrenoceptors.
B. Inhibition of catechol-O-methyltransferase (COMT).
C. Displacement of norepinephrine from storage vesicles and subsequent release via reverse transport through NET.
D. Inhibition of monoamine oxidase (MAO), leading to accumulation of norepinephrine.
Answer: C) Explanation:

Correct ©: Indirect-acting sympathomimetics like amphetamine and tyramine are

taken up into the presynaptic nerve terminal (often via NET). Once inside, they enter synaptic vesicles (displacing NE) or cause
maffy NE to move from vesicles into the cytoplasm. This cytoplasmic NE then exits the neuron via reverse transport through the NET,
increasing NE concentration in the synaptic cleft. This release is
Ca2±independent. (ANS Intro Slide 61; Sympathomimetics Slide 116)
Incorrect (A): This describes direct-acting agonists. While amphetamine has some weak direct action, its primary effect is
indirect.
Incorrect (B & D): While MAO and COMT metabolize NE, these drugs’ primary action is not inhibition of these enzymes.

5. A patient being treated for hypertension with a beta-blocker develops acute

bronchospasm. Which of the following beta-blockers was most likely responsible for this adverse effect?
A. Metoprolol
B. Atenolol
C. Propranolol
D. Esmolol
Answer: C) Explanation:

Correct ©: Propranolol is a non-selective beta-blocker, meaning it blocks both Beta- 1 receptors (in the heart) and Beta-2
receptors. Beta-2 receptors mediate
bronchodilation. Blockade of these receptors in a patient with underlying reactive airway disease (like asthma or COPD) can
precipitate bronchospasm. (Anti-
Adrenergics Slide 119, 120 side effects)
Incorrect (A, B, D): Metoprolol, Atenolol, and Esmolol are Beta-1 selective (“cardioselective”) blockers. While their selectivity is
dose-dependent and can be lost at high doses, they are less likely to cause bronchospasm at therapeutic doses compared to non-
selective agents.
6. The termination of acetylcholine’s action in the synaptic cleft is primarily achieved by:
A. Reuptake into the presynaptic neuron by the choline transporter (CHT).
 B. Diffusion away from the synaptic cleft. certain side effect.
C. Enzymatic hydrolysis by acetylcholinesterase (AChE).
D. Uptake and metabolism by glial cells surrounding the synapse. 12. Which of the following steps in adrenergic neurotransmission is the primary site of action for cocaine?
Answer: C) Explanation: A. Inhibition of tyrosine hydroxylase.
B. Blockade of vesicular monoamine transporter (VMAT).
Correct ©: Acetylcholinesterase (AChE) is a highly efficient enzyme located in the synaptic cleft (and on postsynaptic C. Inhibition of norepinephrine transporter (NET).
membranes) that rapidly hydrolyzes acetylcholine into inactive choline and acetate. This enzymatic degradation is the D. Direct stimulation of postsynaptic adrenoceptors.
primary and most rapid mechanism for terminating ACh’s action. (ANS Intro Slide 50, 55) Answer: C) Explanation:
Incorrect (A): Choline (a product of ACh hydrolysis) is taken back up by CHT, but ACh itself is not significantly reuptaken.
Incorrect (B): Diffusion plays a minor role compared to enzymatic degradation. Incorrect (D): While glial cells can play roles in Correct ©: Cocaine’s primary mechanism for producing sympathomimetic effects is the inhibition of the Norepinephrine
neurotransmitter clearance for other systems (e.g., glutamate), ACh termination is dominated by AChE. Transporter (NET) on the presynaptic membrane. This blocks the reuptake of norepinephrine from the synaptic cleft,
leading to increased NE concentration and prolonged stimulation of postsynaptic adrenoceptors. Cocaine also blocks
7. Which of the following describes the coupling mechanism of Alpha-1 adrenoceptors? dopamine and serotonin transporters. (ANS Intro Slide 62, 70; Sympathomimetics Slide 116)
A. Activation of Gs protein, leading to increased cAMP. Incorrect (A): Metyrosine inhibits tyrosine hydroxylase. Incorrect (B): Reserpine blocks VMAT.
B. Activation of Gi protein, leading to decreased cAMP. Incorrect (D): Cocaine is an indirect-acting sympathomimetic, not a direct receptor agonist.
C. Direct opening of a ligand-gated ion channel.
D. Activation of Gq protein, leading to increased IP3 and DAG. Answer: D) 13. The phenomenon of denervation supersensitivity, where a tissue becomes more responsive to an agonist after its nerve supply is lost, is
Explanation: primarily due to:
A. Decreased enzymatic degradation of the agonist in the synaptic cleft.
Correct (D): Alpha-1 adrenoceptors are coupled to Gq proteins. Activation of Gq B. Up-regulation and increased number of postsynaptic receptors.
stimulates phospholipase C (PLC), which hydrolyzes PIP2 into inositol trisphosphate (IP3) and diacylglycerol (DAG). IP3 causes C. Enhanced synthesis and release of the endogenous neurotransmitter.
release of intracellular Ca2+, and DAG activates Protein Kinase C (PKC). (ANS Intro Slide 83, 84) D. Proliferation of presynaptic nerve terminals.
Incorrect (A): This describes Beta-adrenoceptors (β1, β2, β3). Answer: B) Explanation:
Incorrect (B): This describes Alpha-2 adrenoceptors and Muscarinic M2/M4 receptors.
Incorrect ©: This describes ionotropic receptors like nicotinic receptors. Correct (B): When a tissue is deprived of its normal nerve input (denervation), the postsynaptic cells often compensate by
increasing the number (up-regulation) and/or sensitivity of their receptors for the neurotransmitter that is no longer being
8. A drug that produces its effects by mimicking acetylcholine at autonomic ganglia and the adrenal medulla, but not significantly at postganglionic released adequately. This makes the tissue hyperresponsive to exogenously administered agonists. (ANS Intro Slide 101)
parasympathetic effector sites, would be classified as primarily a: Incorrect (A): Enzyme levels might change, but receptor up-regulation is the primary mechanism.
A. Muscarinic agonist. Incorrect ©: Denervation means loss of endogenous neurotransmitter release from that nerve.
B. Nicotinic agonist (Nn selective or non-selective but potent at Nn). Incorrect (D): Denervation involves degeneration of terminals, not proliferation.
C. Acetylcholinesterase inhibitor. 14. A patient receives an IV infusion of a drug that causes a significant increase in mean arterial pressure and a profound reflex bradycardia. This
D. Muscarinic antagonist. Answer: B) Explanation: drug is most likely a potent agonist at which receptors?
A. Beta-1 and Beta-2 adrenoceptors.
Correct (B): Autonomic ganglia and the adrenal medulla contain Nicotinic (Nn) cholinergic receptors. Postganglionic B. Muscarinic M2 cholinoceptors.
parasympathetic effector sites (smooth muscle, glands, heart) primarily contain Muscarinic (M) receptors. A drug mimicking ACh C. Alpha-1 adrenoceptors.
at ganglia/adrenal medulla but not effectors is acting on Nn receptors. Nicotine itself or selective Nn agonists would fit this D. Nicotinic Nn cholinoceptors.
profile. (ANS Intro Slide 71, 79, 80) Answer: C) Explanation:
Incorrect (A): Muscarinic agonists primarily target effector sites.
Incorrect ©: AChE inhibitors would enhance ACh action at all cholinergic sites (Nn, Nm, M). Correct ©: Potent Alpha-1 adrenoceptor agonism causes widespread
Incorrect (D): Muscarinic antagonists block effects at M receptors. vasoconstriction, leading to a significant increase in peripheral vascular resistance and thus a rise in mean arterial pressure.
This acute hypertension then triggers the baroreceptor reflex, leading to increased vagal tone and decreased sympathetic tone
9. The “fight-or-flight” response is characterized by all of the following physiological changes EXCEPT: to the heart, resulting in reflex bradycardia. Norepinephrine exhibits this profile. (ANS Intro Slide 97, 98)
A. Increased heart rate and contractility. Incorrect (A): Beta-1 agonism would increase HR directly; Beta-2 agonism would cause vasodilation and lower BP.
B. Dilation of pupils (mydriasis). Incorrect (B): Muscarinic M2 agonists cause bradycardia and hypotension.
C. Increased gastrointestinal motility and secretion. Incorrect (D): Nicotinic Nn agonists (ganglionic stimulants) would activate both
D. Bronchodilation. Answer: C) Explanation: sympathetic and parasympathetic systems, leading to complex, often unpredictable cardiovascular effects (e.g., tachycardia and
hypertension).
Incorrect (C is the exception): The fight-or-flight response, mediated by the sympathetic nervous system, generally decreases gastrointestinal
motility and 15. The rate-limiting enzyme in the synthesis of acetylcholine is:
secretions. Energy and blood flow are shunted away from the GI tract to muscles and vital organs. (ANS Intro Slide 19, 20) A. Acetylcholinesterase (AChE).
Correct (A, B, D): Increased heart rate/contractility (β1), mydriasis (α1), and bronchodilation (β2) are all characteristic features B. Choline acetyltransferase (ChAT), dependent on choline uptake.
of the sympathetic stress response. C. Vesicular acetylcholine transporter (VAChT).
D. L-amino acid decarboxylase.
10. What is the primary reason for the short duration of action of intravenously administered acetylcholine?
Answer: B) Explanation:
A. Rapid uptake into presynaptic nerve terminals.
B. Extensive binding to plasma proteins. Correct (B): While Choline Acetyltransferase (ChAT) is the enzyme that synthesizes ACh from choline and acetyl-CoA, the overall
C. Rapid hydrolysis by acetylcholinesterase and plasma butyrylcholinesterase. rate of ACh synthesis is primarily
D. Slow dissociation from muscarinic and nicotinic receptors. limited by the availability of choline, which depends on its active uptake into the presynaptic neuron by the high-affinity Choline
Answer: C) Explanation: Transporter (CHT). Thus, choline
uptake is considered the true rate-limiting step, and ChAT’s activity is dependent on this. (ANS Intro Slide 52)
Correct ©: Acetylcholine is very rapidly hydrolyzed in the blood and tissues by both acetylcholinesterase (AChE, present in RBCs
Incorrect (A): AChE degrades ACh. Incorrect ©: VAChT stores ACh in vesicles.
and at synapses) and, more significantly for IV administration, by plasma butyrylcholinesterase (BuChE). This enzymatic
Incorrect (D): L-amino acid decarboxylase is involved in catecholamine and serotonin synthesis.
degradation leads to an extremely short half-life (seconds to minutes). (ANS Intro Slide 55, 56; Cholinomimetics Slide 105)
Incorrect (A): ACh is not significantly reuptaken presynaptically; its breakdown product, choline, is. 16. Activation of Gq protein-coupled receptors, such as Muscarinic M3 or Alpha-1 adrenoceptors, leads to the intracellular production of which
Incorrect (B): ACh does not bind extensively to plasma proteins. second messenger(s)?
Incorrect (D): Receptor dissociation is part of the action, but the enzymatic breakdown is the primary factor limiting its duration A. Cyclic AMP (cAMP) only.
in circulation. B. Cyclic GMP (cGMP) only.
C. Inositol trisphosphate (IP3) and Diacylglycerol (DAG).
11. A patient with asthma inadvertently receives a high dose of a non-selective beta-agonist. Which of the following adverse effects is most likely to be D. Nitric Oxide (NO). Answer: C) Explanation:
prominent?
A. Bradycardia. Correct ©: Receptors coupled to Gq proteins activate the enzyme Phospholipase C (PLC). PLC hydrolyzes phosphatidylinositol
B. Bronchoconstriction. 4,5-bisphosphate (PIP2) in the cell membrane to produce two second messengers: Inositol trisphosphate (IP3) and
C. Tachycardia and muscle tremor. Diacylglycerol (DAG). IP3 mobilizes intracellular Ca2+, and DAG activates Protein Kinase C. (ANS Intro Slide 73, 83, 84)
D. Hypotension. Answer: C) Explanation: Incorrect (A): cAMP is produced by activation of Gs (e.g., Beta receptors) or inhibited by Gi (e.g., M2, Alpha-2 receptors).
Incorrect (B): cGMP is produced by guanylyl cyclase (often activated by NO or natriuretic peptides).
Correct ©: A non-selective beta-agonist (like isoproterenol) will stimulate: Incorrect (D): NO is a signaling molecule but is typically generated by NO synthase, which can be activated downstream of Ca2+
Beta-1 receptors in the heart, causing tachycardia and increased contractility. mobilization (e.g., by M3 receptor activation in endothelial cells).
Beta-2 receptors in bronchial smooth muscle (therapeutic effect:
17. Which of the following autonomic ganglia are characterized by long preganglionic fibers and very short postganglionic fibers that innervate
bronchodilation), skeletal muscle blood vessels (vasodilation), and skeletal muscle itself (can cause tremor). effector organs directly or are embedded within them?
Thus, tachycardia (from β1) and muscle tremor (from β2 stimulation of skeletal muscle) are expected prominent side A. Sympathetic paravertebral ganglia.
effects. B. Sympathetic prevertebral ganglia.
Incorrect (A): Bradycardia would not occur; tachycardia is expected. C. Parasympathetic terminal ganglia.
Incorrect (B): Bronchodilation is the therapeutic effect; bronchoconstriction would be caused by beta-blockers. D. Adrenal medulla. Answer: C) Explanation:
Incorrect (D): Beta-2 stimulation causes vasodilation, which can lead to a decrease in diastolic blood pressure (hypotension), but
the β1-mediated increase in cardiac output can sometimes maintain or increase systolic BP. Tachycardia is a more direct and Correct ©: Parasympathetic preganglionic neurons originate in the craniosacral regions and their axons travel a long distance to
 synapse in terminal ganglia located very close to, or within the walls of, the target effector organs. Consequently, the B. Alpha-1 adrenergic receptors.
parasympathetic postganglionic fibers are very short. (ANS Intro Slide 13, 14) C. Muscarinic cholinergic receptors.
Incorrect (A & B): Sympathetic ganglia (paravertebral and prevertebral) are D. Nicotinic cholinergic receptors.
generally located closer to the spinal cord, resulting in short preganglionic and long postganglionic fibers. Answer: C) Explanation:
Incorrect (D): The adrenal medulla is a modified sympathetic ganglion innervated by preganglionic fibers, but it releases
hormones into the blood rather than having short postganglionic fibers innervating an organ. Correct ©: Tricyclic antidepressants (TCAs) are known to have significant anticholinergic (antimuscarinic) properties in addition
to their primary action of blocking norepinephrine and serotonin reuptake. The symptoms described –
18. Pralidoxime is administered as an antidote in organophosphate poisoning. Its primary beneficial action involves: tachycardia (blocking vagal tone), dry mouth (blocking salivary secretion), blurred vision (cycloplegia/mydriasis), and urinary
A. Blocking muscarinic receptors to counteract excessive ACh stimulation. retention – are classic manifestations of muscarinic receptor blockade (atropine-like effects). (Indirect-Acting Sympathomimetics
B. Competitively inhibiting acetylcholinesterase to prevent further binding of the organophosphate. Slide 116 - TCA action on NET/SERT; Antimuscarinic side effects Slide 113 - general anticholinergic toxicities)
C. Reactivating organophosphate-inhibited acetylcholinesterase, particularly at nicotinic sites. Incorrect (A): Beta-1 blockade would cause bradycardia.
D. Enhancing the metabolic degradation of the organophosphate toxin. Incorrect (B): Alpha-1 blockade primarily causes vasodilation and postural hypotension.
Answer: C) Explanation: Incorrect (D): Nicotinic blockade would lead to ganglionic blockade or neuromuscular blockade, which have different symptom
profiles.
Correct ©: Organophosphates form a stable, often covalent bond with the active site of acetylcholinesterase (AChE), irreversibly 24. The conversion of DOPA to dopamine in adrenergic and dopaminergic neurons is catalyzed by which enzyme?
inhibiting it (if not treated quickly). A. Tyrosine hydroxylase (TH).
Pralidoxime (an oxime) works by nucleophilically attacking the phosphorus atom of the organophosphate, displacing it from the B. L-Amino acid decarboxylase (AADC) / DOPA decarboxylase.
enzyme’s active site and thereby reactivating AChE. This reactivation is most effective at the neuromuscular junction (nicotinic C. Dopamine β-hydroxylase (DBH).
sites) and is time-sensitive (must be given before “aging” of the D. Phenylethanolamine N-methyltransferase (PNMT).
phosphorylated enzyme occurs). (Cholinomimetics Slide 105 - implication; standard pharmacology) Answer: B) Explanation:
Incorrect (A): Atropine blocks muscarinic receptors. Incorrect (B): Pralidoxime reactivates, it doesn’t
inhibit AChE. Correct (B): L-Amino acid decarboxylase (AADC), also commonly called DOPA
Incorrect (D): It does not enhance organophosphate metabolism. decarboxylase, is the enzyme that catalyzes the decarboxylation of DOPA to form dopamine. This step occurs in the cytoplasm.
(ANS Intro Slide 59, 60)
19. The baroreceptor reflex plays a crucial role in the short-term regulation of arterial blood pressure. A sudden increase in blood pressure would lead Incorrect (A): TH converts tyrosine to DOPA.
to which of the following reflex autonomic adjustments? Incorrect ©: DBH converts dopamine to norepinephrine (inside vesicles). Incorrect (D): PNMT converts norepinephrine to
A. Increased sympathetic outflow and decreased parasympathetic outflow. epinephrine (mainly in adrenal medulla).
B. Decreased sympathetic outflow and increased parasympathetic outflow.
C. Increased sympathetic outflow and increased parasympathetic outflow. 25. An experimental drug is found to increase heart rate, cause bronchodilation, and
D. Decreased sympathetic outflow and decreased parasympathetic outflow. promote glycogenolysis in the liver. These effects suggest the drug is primarily an agonist at which receptor subtype(s)?
Answer: B) Explanation: A. Alpha-1 and Muscarinic M3.
B. Alpha-2 and Beta-1.
Correct (B): An increase in blood pressure stretches baroreceptors in the carotid sinus and aortic arch. This increases their firing C. Beta-1 and Beta-2.
rate, sending signals to the D. Muscarinic M2 and Beta-2.
brainstem (NTS). The NTS then integrates this information and orchestrates a reflex response aimed at lowering BP: it Answer: C) Explanation:
decreases sympathetic outflow (reducing heart rate, contractility, and vasoconstriction) and increases parasympathetic (vagal)
outflow to the heart (slowing heart rate). (ANS Intro Slide 97, 98, 100) Correct ©:
Incorrect (A, C, D): These combinations do not represent the homeostatic response to high blood pressure. Increased heart rate is primarily mediated by Beta-1 receptor stimulation. Bronchodilation is primarily mediated by Beta-2
receptor stimulation.
20. A patient is treated with a drug that enhances the release of norepinephrine from Hepatic glycogenolysis is also significantly stimulated by Beta-2 receptors (and to some extent alpha receptors).
sympathetic nerve terminals and also directly stimulates alpha and beta adrenoceptors. This drug is best classified as a(n): Thus, combined Beta-1 and Beta-2 agonism (like isoproterenol or epinephrine) would produce this profile of effects.
A. Direct-acting sympathomimetic. Incorrect (A): Alpha-1 causes vasoconstriction; M3 causes bronchoconstriction and gland secretion.
B. Indirect-acting sympathomimetic (releasing agent). Incorrect (B): Alpha-2 centrally reduces sympathetic outflow; Beta-1 increases HR. Incorrect (D): M2 slows heart rate; Beta-2
C. Mixed-acting sympathomimetic. causes bronchodilation.
D. Non-selective adrenoceptor antagonist.
Answer: C) Explanation: 26. In the context of the autonomic nervous system, which of the following structures is considered a “modified sympathetic ganglion” that
releases hormones into the
Correct ©: Drugs that have both direct receptor stimulating activity (binding to and activating adrenoceptors) and indirect bloodstream?
activity (causing the release of endogenous norepinephrine) are classified as mixed-acting sympathomimetics. Ephedrine and A. Celiac ganglion.
pseudoephedrine are classic examples. (Sympathomimetics Slide 116) B. Superior cervical ganglion.
Incorrect (A): Direct-acting agents only bind to receptors. C. Adrenal medulla.
Incorrect (B): Indirect-acting releasing agents primarily cause NE release without significant direct receptor agonism. D. Otic ganglion. Answer: C) Explanation:
Incorrect (D): This describes a blocker, not a stimulant.
Correct ©: The adrenal medulla is embryologically derived from neural crest cells, similar to postganglionic sympathetic
21. The primary neurotransmitter released by most postganglionic parasympathetic neurons is: neurons. It is innervated directly by
A. Norepinephrine. preganglionic sympathetic fibers that release acetylcholine. In response, the
B. Epinephrine. chromaffin cells of the adrenal medulla release epinephrine (~80%) and
C. Dopamine. norepinephrine (~20%) into the systemic circulation, where they act as hormones. Thus, it functions as a modified sympathetic
D. Acetylcholine. Answer: D) Explanation: ganglion. (ANS Intro Slide 12, 15)
Correct (D): Acetylcholine (ACh) is the neurotransmitter released by almost all Incorrect (A, B): Celiac and superior cervical ganglia are standard sympathetic ganglia where preganglionic fibers synapse
postganglionic parasympathetic fibers, acting on muscarinic receptors on effector organs. (ANS Intro Slide 5, 15, 28) with postganglionic neurons that release neurotransmitters locally.
Incorrect (A, B, C): Norepinephrine is released by most postganglionic sympathetic neurons. Epinephrine is primarily a Incorrect (D): The otic ganglion is a parasympathetic ganglion.
hormone from the adrenal medulla. Dopamine is a neurotransmitter in specific pathways (e.g., CNS, some peripheral
sympathetic nerves like renal). 27. Which of the following statements accurately describes the relative lengths of
preganglionic and postganglionic fibers in the sympathetic versus parasympathetic nervous systems?
22. Which of the following is a characteristic feature of chemical synapses that distinguishes them from electrical synapses? A. Sympathetic: long preganglionic, short postganglionic; Parasympathetic: short preganglionic, long postganglionic.
A. Bidirectional transmission of signals. B. Sympathetic: short preganglionic, long postganglionic; Parasympathetic: long preganglionic, short postganglionic.
B. Minimal synaptic delay. C. Both systems have short preganglionic and long postganglionic fibers.
C. Presence of neurotransmitter-filled vesicles in the presynaptic terminal. D. Both systems have long preganglionic and short postganglionic fibers.
D. Direct cytoplasmic continuity between pre- and postsynaptic cells. Answer: B) Explanation:
Answer: C) Explanation:
Correct (B):
Correct ©: Chemical synapses utilize neurotransmitters stored in presynaptic vesicles. The release of these vesicles (exocytosis) Sympathetic: Preganglionic neurons originate in the thoracolumbar spinal cord and synapse in ganglia relatively close to
is a hallmark of chemical the spinal cord (paravertebral chain or prevertebral ganglia). This results in short preganglionic fibers and long
transmission. (ANS Intro Slide 37, 39) postganglionic fibers that travel to target organs.
Incorrect (A): Chemical transmission is unidirectional (pre- to postsynaptic). Electrical synapses can be bidirectional. Parasympathetic: Preganglionic neurons originate in the craniosacral regions and travel a long distance to synapse in terminal ganglia
Incorrect (B): Chemical synapses have a significant synaptic delay (0.5-5 ms) due to the steps of release, diffusion, and receptor located very near or within the target organs. This results in long preganglionic fibers and very short postganglionic fibers. (ANS Intro
binding. Electrical synapses have minimal delay. (ANS Intro Slide 38) Slide 14)
Incorrect (D): Electrical synapses (gap junctions) have direct cytoplasmic continuity. Chemical synapses have a synaptic cleft Incorrect (A, C, D): These describe incorrect combinations.
separating the cells.
28. A key difference between the somatic nervous system and the autonomic nervous system is that:
23. A patient with an overdose of a tricyclic antidepressant (TCA) develops severe A. The somatic nervous system involves a two-neuron chain to its effector, while the ANS uses a single neuron.
tachycardia, dry mouth, blurred vision, and urinary retention. These adverse effects are primarily due to the TCA’s blockade of which B. The somatic nervous system exclusively uses acetylcholine as its neurotransmitter at the effector junction, while the
type of receptor? ANS uses acetylcholine and norepinephrine.
A. Beta-1 adrenergic receptors. C. The somatic nervous system innervates smooth muscle and glands, while the ANS innervates skeletal muscle.
 D. Somatic motor neurons are unmyelinated, while autonomic preganglionic neurons are heavily myelinated. Incorrect (B): These are primarily Beta-2 effects. Incorrect (D): These are Alpha-1 effects.
Answer: B) Explanation:
34. Which step in the synthesis of norepinephrine is considered rate-limiting and is inhibited by metyrosine?
Correct (B): Somatic motor neurons release acetylcholine (ACh) at the A. Conversion of DOPA to dopamine by L-amino acid decarboxylase.
neuromuscular junction to act on Nm receptors on skeletal muscle. The ANS uses ACh at all preganglionic synapses and at B. Transport of dopamine into synaptic vesicles by VMAT.
postganglionic parasympathetic synapses; however, most postganglionic sympathetic neurons release norepinephrine (NE). C. Conversion of tyrosine to DOPA by tyrosine hydroxylase.
(ANS Intro Slide 5, 15) D. Hydroxylation of dopamine to norepinephrine by dopamine β-hydroxylase.
Incorrect (A): Somatic NS uses a single neuron from CNS to effector. ANS uses a two- neuron chain. Answer: C) Explanation:
Incorrect ©: Somatic NS innervates skeletal muscle. ANS innervates smooth muscle, cardiac muscle, and glands.
Incorrect (D): Somatic motor neurons are heavily myelinated. Autonomic Correct ©: The conversion of tyrosine to dihydroxyphenylalanine (DOPA) catalyzed by the enzyme tyrosine hydroxylase (TH) is
preganglionic neurons are lightly myelinated, and postganglionic autonomic neurons are unmyelinated. the slowest, rate-limiting step in the entire catecholamine biosynthesis pathway. Metyrosine is a competitive inhibitor of TH.
(ANS Intro Slide 58, 60)
29. A drug that inhibits acetylcholinesterase would be expected to potentiate the effects of acetylcholine at all of the following sites EXCEPT: Incorrect (A): This step is catalyzed by AADC. Incorrect (B): This is vesicular storage, not
A. Postganglionic parasympathetic neuroeffector junctions. synthesis.
B. Autonomic ganglia. Incorrect (D): This step is catalyzed by DBH inside vesicles.
C. Neuromuscular junction.
D. Postganglionic sympathetic neuroeffector junctions innervating most blood vessels. 35. Administration of a selective Alpha-2 adrenergic agonist, like clonidine, results in a decrease in blood pressure primarily through which
Answer: D) Explanation: mechanism?
A. Direct vasodilation of peripheral arterioles by activating postsynaptic alpha-2 receptors.
Correct (D is the exception): Acetylcholinesterase inhibitors increase ACh levels. B. Blockade of norepinephrine reuptake at sympathetic nerve terminals.
A (Parasympathetic effectors): ACh is the transmitter, so effects are potentiated. C. Activation of alpha-2 adrenoceptors in the brainstem (CNS), leading to reduced sympathetic outflow.
B (Autonomic ganglia): ACh is the preganglionic transmitter, so effects are potentiated. D. Competitive antagonism of alpha-1 adrenoceptors on vascular smooth muscle.
C (Neuromuscular junction): ACh is the transmitter, so effects are potentiated. Answer: C) Explanation:
D (Most sympathetic vascular neuroeffector junctions): The neurotransmitter here is norepinephrine, not acetylcholine.
Therefore, an AChE inhibitor would have no direct effect on potentiating transmission at these specific adrenergic Correct ©: Clonidine and other centrally acting alpha-2 agonists lower blood
junctions. (The exception is sympathetic cholinergic nerves to sweat pressure by stimulating alpha-2 adrenoceptors located in the vasomotor centers of the brainstem (e.g., nucleus of the solitary
glands/some vessels, but “most blood vessels” are adrenergic). (ANS Intro Slide 28, 29; Cholinomimetics Slide 108) tract). Activation of these receptors reduces sympathetic outflow from the CNS to the peripheral cardiovascular system, leading
to decreased heart rate, cardiac output, and peripheral vascular resistance. (ANS Intro Slide 85; Sympathomimetics Slide 117)
30. The primary mechanism by which the effects of norepinephrine are terminated in the synaptic cleft of most sympathetic neuroeffector Incorrect (A): While some peripheral postsynaptic alpha-2 receptors can cause
junctions is: vasoconstriction, the predominant antihypertensive effect of clonidine is central. Incorrect (B): This describes drugs like cocaine
A. Enzymatic degradation by catechol-O-methyltransferase (COMT) in the cleft. or TCAs.
B. Enzymatic degradation by monoamine oxidase (MAO) in the cleft. Incorrect (D): This describes alpha-1 blockers. Clonidine is an agonist.
C. Diffusion away from the synaptic cleft and uptake by extraneuronal cells.
D. Reuptake into the presynaptic nerve terminal by the norepinephrine transporter (NET). 36. A patient with acute decompensated heart failure and low cardiac output is given
Answer: D) Explanation: dobutamine. The primary beneficial effect of dobutamine in this setting is due to its relatively selective agonist activity at:
A. Alpha-1 adrenoceptors, causing increased peripheral resistance.
Correct (D): The predominant mechanism (accounting for ~87-92%) for terminating the action of released norepinephrine is B. Beta-1 adrenoceptors, causing increased myocardial contractility.
active reuptake back into the presynaptic C. Beta-2 adrenoceptors, causing significant bronchodilation.
sympathetic nerve terminal via the Norepinephrine Transporter (NET or Uptake 1). (ANS Intro Slide 62, 70) D. Dopamine D1 receptors, causing renal vasodilation.
Incorrect (A & B): COMT and MAO are involved in metabolizing NE, but COMT acts Answer: B) Explanation:
largely extraneuronally/systemically, and MAO acts primarily intra-neuronally after reuptake. They are not the primary rapid
termination mechanisms in the cleft. Correct (B): Dobutamine is a sympathomimetic primarily used for its relatively
Incorrect ©: Diffusion and extraneuronal uptake (Uptake 2) are secondary, minor mechanisms for NE removal from the cleft. selective Beta-1 adrenergic agonist activity. Beta-1 stimulation increases myocardial contractility (positive inotropic effect) and,
to a lesser extent, heart rate, thereby improving cardiac output in acute heart failure. While it has some β2 and α1
31. Which of the following receptors is a ligand-gated ion channel?
activity, the β1 effect dominates its cardiac use. (Sympathomimetics Slide 116 list, Slide 117 uses)
A. Muscarinic M2 receptor.
Incorrect (A): Increased peripheral resistance would worsen heart failure. Incorrect ©: While it has some β2 activity,
B. Beta-2 adrenoceptor.
bronchodilation is not its primary use in heart failure.
C. Alpha-1 adrenoceptor.
Incorrect (D): Dopamine itself has D1 activity; dobutamine’s primary cardiac effects are β1-mediated.
D. Nicotinic Nm receptor. Answer: D)
Explanation: 37. Which of the following is a unique characteristic of the sympathetic innervation of the adrenal medulla compared to other sympathetic
pathways?
Correct (D): Nicotinic acetylcholine receptors (both Nm at the neuromuscular junction and Nn in ganglia/CNS) are ligand-gated A. Postganglionic fibers release norepinephrine.
ion channels. Binding of acetylcholine directly opens an integral ion pore. (ANS Intro Slide 71, 79, 80) B. Preganglionic fibers are unmyelinated.
Incorrect (A, B, C): Muscarinic M2 receptors, Beta-2 adrenoceptors, and Alpha-1 adrenoceptors are all G-protein coupled C. Preganglionic fibers synapse directly with effector cells (chromaffin cells) that release hormones into the blood.
receptors (GPCRs), not ligand-gated ion channels. They signal via intracellular second messenger pathways. (ANS Intro Slide 72, D. It is part of the parasympathetic nervous system.
82, 83, 86) Answer: C) Explanation:
(Continuing to Q51-100) Correct ©: Preganglionic sympathetic fibers pass through the sympathetic chain and celiac ganglion (often without
synapsing) to directly innervate the chromaffin cells of the adrenal medulla. These chromaffin cells are modified
32. A patient inadvertently ingests a substance that irreversibly inhibits acetylcholinesterase.
postganglionic
Which of the following signs and symptoms would be LEAST consistent with this poisoning?
neurons that, upon stimulation by acetylcholine from the preganglionic nerve, release epinephrine and norepinephrine into the
A. Miosis (pupil constriction).
bloodstream, acting as hormones. (ANS Intro Slide 12, 15, 30)
B. Bronchoconstriction and wheezing.
Incorrect (A): Chromaffin cells release Epi/NE as hormones; there isn’t a typical postganglionic neuron releasing NE locally.
C. Muscle fasciculations and paralysis.
Incorrect (B): Preganglionic fibers in the ANS are generally lightly myelinated. Incorrect (D): The adrenal medulla is
D. Dry mouth and tachycardia. Answer: D)
innervated by the sympathetic nervous system.
Explanation:
38. The “rest-and-digest” functions of the body are primarily mediated by which division of the autonomic nervous system?
Least Consistent (D): Irreversible AChE inhibition leads to accumulation of ACh at all cholinergic synapses, causing excessive
A. Somatic nervous system.
stimulation. Dry mouth and tachycardia are signs of anticholinergic (muscarinic blockade) effects, the opposite of what would
B. Sympathetic nervous system.
be expected. ACh excess causes increased salivation (muscarinic) and
bradycardia (muscarinic M2 on heart).
C. Parasympathetic nervous system.
Consistent (A, B, C): Miosis (muscarinic M3 on iris sphincter), bronchoconstriction (muscarinic M3 on bronchial smooth muscle), D. Enteric nervous system independently.
and muscle fasciculations/paralysis (nicotinic Nm overstimulation at NMJ leading to depolarization block) are all characteristic Answer: C) Explanation:
of AChE inhibitor poisoning. (Cholinomimetics Slide 109)
Correct ©: The parasympathetic nervous system is responsible for promoting
33. The activation of Beta-3 adrenoceptors leads primarily to: processes associated with energy conservation, digestion, absorption of nutrients, and bodily restoration, often summarized as
A. Increased heart rate and contractility. “rest-and-digest” activities. (ANS Intro Slide 3, 21)
B. Bronchodilation and vasodilation in skeletal muscle. Incorrect (A): Somatic NS controls voluntary muscle.
C. Lipolysis in adipose tissue and relaxation of the bladder detrusor muscle. Incorrect (B): Sympathetic NS mediates “fight-or-flight” responses.
D. Vasoconstriction and mydriasis. Incorrect (D): The ENS manages gut function but is heavily modulated by both sympathetic and parasympathetic input for overall
Answer: C) Explanation: “rest-and-digest” state.

Correct ©: Beta-3 adrenoceptors are primarily located in adipose tissue, where their activation stimulates lipolysis (breakdown 39. The enzyme responsible for converting norepinephrine to epinephrine primarily in the adrenal medulla is:
of fat). They are also found on the A. Tyrosine hydroxylase.
detrusor muscle of the urinary bladder, where their activation promotes relaxation. (ANS Intro Slide 82, 86) B. Dopamine β-hydroxylase.
Incorrect (A): These are Beta-1 effects. C. Monoamine oxidase (MAO).
 D. Phenylethanolamine N-methyltransferase (PNMT). Answer: D) C. Decreased number of functional receptors on the cell surface due to internalization and/or degradation.
Explanation: D. Mutation of the receptor gene leading to a non-functional protein.
Answer: C) Explanation:
Correct (D): Phenylethanolamine N-methyltransferase (PNMT) is the enzyme that catalyzes the methylation of norepinephrine
to form epinephrine. This conversion occurs mainly in the cytoplasm of adrenal medullary chromaffin cells (and to a Correct ©: Chronic or excessive stimulation of receptors by an agonist often leads to adaptive changes aimed at reducing the
lesser extent in certain brain neurons). (ANS Intro Slide 59, 60) Incorrect (A): TH converts tyrosine to DOPA. cell’s responsiveness. This includes receptor desensitization (uncoupling from G-proteins, often via phosphorylation by GRKs and
Incorrect (B): DBH converts dopamine to norepinephrine. Incorrect ©: MAO degrades catecholamines. arrestin binding), receptor internalization (endocytosis, removing receptors from
the cell surface), and eventually receptor degradation, collectively leading to a decreased number of functional receptors. This is
40. In the baroreceptor reflex arc, increased firing from baroreceptors due to elevated blood pressure directly signals to which primary integrating a key mechanism of drug
center in the brainstem? tolerance. (ANS Intro Slide 101, Pharmacodynamics Slide 209)
A. Hypothalamus. Incorrect (A): Increased synthesis would be up-regulation (seen with chronic antagonist).
B. Nucleus of the solitary tract (NTS). Incorrect (B): Downregulation involves decreased coupling or receptor number.
C. Celiac ganglion. Incorrect (D): Mutations are genetic changes, not typically the mechanism of pharmacologically induced downregulation.
D. Cerebellum. Answer: B) Explanation:
46. A patient experiences significant vasodilation, a drop in diastolic blood pressure, and reflex tachycardia after administration of a drug. These
Correct (B): Afferent signals from arterial baroreceptors (in the carotid sinus and aortic arch) travel via the glossopharyngeal effects are blocked by
(IX) and vagus (X) nerves to the Nucleus of the Solitary Tract (NTS) in the medulla oblongata (brainstem). The NTS is the propranolol. The drug most likely activated which receptors?
primary site of termination and integration for these visceral afferent inputs. (ANS Intro Slide 98, 100) A. Alpha-1 adrenoceptors.
Incorrect (A): The hypothalamus is a higher control center for the ANS but the NTS is the first central relay for the baroreflex. B. Muscarinic M3 cholinoceptors.
Incorrect ©: The celiac ganglion is a peripheral sympathetic ganglion. Incorrect (D): The cerebellum is primarily C. Beta-2 adrenoceptors (and possibly some Beta-1 for reflex tachycardia).
involved in motor coordination. D. Dopamine D1 receptors.
Answer: C) Explanation:
41. A drug that acts as a selective M3 muscarinic receptor antagonist would be most useful for treating:
A. Bradycardia. Correct ©: Significant vasodilation leading to a drop in diastolic BP is a hallmark of Beta-2 adrenoceptor activation (e.g., in
B. Myasthenia gravis. skeletal muscle vascular beds). The
C. Overactive bladder (OAB). subsequent reflex tachycardia is a compensatory response to the hypotension.
D. Glaucoma. Answer: C) Explanation: Propranolol, a non-selective beta-blocker, would block these Beta-2 effects (and also any Beta-1 component contributing to the
reflex or direct cardiac stimulation). (ANS Intro Slide 86, 87)
Correct ©: M3 muscarinic receptors are predominant in mediating detrusor muscle contraction in the urinary bladder. Selective
Incorrect (A): Alpha-1 activation causes vasoconstriction.
M3 antagonists (like darifenacin, Incorrect (B): Muscarinic M3 activation can cause vasodilation (via NO), but the reflex tachycardia and blockade by propranolol
solifenacin, oxybutynin, tolterodine) relax the detrusor muscle, increase bladder capacity, and reduce urinary urgency and
point more strongly to beta- adrenergic mechanisms.
frequency, making them useful for
Incorrect (D): Dopamine D1 receptor activation causes renal and mesenteric vasodilation, but the profile described fits Beta-2
treating overactive bladder. (Anticholinergics Slide 112) agonism best, especially considering the propranolol blockade.
Incorrect (A): Bradycardia would be treated with a muscarinic antagonist like atropine (M2 blockade), or a beta-agonist.
Incorrect (B): Myasthenia gravis is treated with AChE inhibitors. 47. Which of the following neurotransmitters is synthesized and stored primarily within synaptic vesicles in adrenergic neurons, rather than being
synthesized in the cytoplasm and then transported into vesicles?
Incorrect (D): Glaucoma is often treated with muscarinic agonists (like pilocarpine) or beta-blockers, not M3 antagonists which
A. Dopamine.
could worsen some forms of glaucoma.
B. Norepinephrine (synthesis from dopamine occurs in vesicles).
42. The ability of cocaine to produce intense sympathomimetic effects (e.g., tachycardia, hypertension, mydriasis) is primarily due to its action as C. Epinephrine.
a potent inhibitor of: D. Tyrosine. Answer: B) Explanation:
A. Vesicular monoamine transporter (VMAT).
B. Monoamine oxidase (MAO). Correct (B): In adrenergic neurons, tyrosine is converted to DOPA, and DOPA to
C. Norepinephrine transporter (NET), Dopamine transporter (DAT), and Serotonin transporter (SERT). dopamine in the cytoplasm. Dopamine is then transported into synaptic vesicles by VMAT. Inside the vesicles, dopamine is
D. Postsynaptic beta-1 adrenoceptors. converted to norepinephrine by the enzyme dopamine β-hydroxylase (DBH), which is located within the vesicles. (ANS Intro
Answer: C) Explanation: Slide 59, 60)
Incorrect (A): Dopamine is synthesized in the cytoplasm.
Correct ©: Cocaine’s primary mechanism is the blockade of reuptake transporters for monoamines. It potently inhibits NET Incorrect ©: Epinephrine is synthesized from norepinephrine, primarily in the cytoplasm of adrenal medullary cells (NE moves
(norepinephrine), DAT (dopamine), and SERT (serotonin), leading to increased concentrations of these neurotransmitters in
out of vesicles, is converted to Epi, then Epi might be re-vesicularized).
their respective synaptic clefts and thus enhanced postsynaptic receptor
Incorrect (D): Tyrosine is the precursor amino acid taken up from extracellular fluid.
stimulation. The sympathomimetic cardiovascular effects are mainly due to NET inhibition. (ANS Intro Slide 62;
Sympathomimetics Slide 116) 48. The primary mechanism by which organophosphate insecticides exert their toxicity is:
Incorrect (A): Reserpine blocks VMAT. Incorrect (B): MAOIs inhibit MAO. A. Direct blockade of nicotinic acetylcholine receptors.
Incorrect (D): Cocaine is not a direct receptor agonist or antagonist. B. Irreversible activation of muscarinic acetylcholine receptors.
C. Irreversible inhibition of acetylcholinesterase.
43. Which neurotransmitter is released by sympathetic postganglionic neurons innervating eccrine sweat glands? D. Depletion of acetylcholine stores from presynaptic terminals.
A. Norepinephrine. Answer: C) Explanation:
B. Epinephrine.
C. Acetylcholine. Correct ©: Organophosphates are potent, irreversible inhibitors of acetylcholinesterase (AChE). They phosphorylate the active
D. Serotonin. Answer: C) Explanation: site of the enzyme, rendering it non-functional. This leads to accumulation of acetylcholine at all cholinergic synapses
(muscarinic and nicotinic), causing excessive and prolonged stimulation, resulting in cholinergic crisis. (Cholinomimetics Slide
Correct ©: This is a key exception to the rule that sympathetic postganglionic 105, 109 implications)
neurons are adrenergic. The sympathetic fibers innervating eccrine sweat glands are cholinergic; they release acetylcholine
Incorrect (A & B): They don’t directly block or activate receptors; they prevent ACh breakdown.
(ACh), which acts on Muscarinic (M3) receptors on the sweat glands to stimulate sweat production. (ANS Intro Slide 15, 28, 29,
Incorrect (D): They cause an excess of ACh, not depletion.
30)
Incorrect (A & B): NE/Epi are released by most other sympathetic postganglionics. Incorrect (D): Serotonin is not the primary 49. Botulinum toxin and Tetanus toxin both interfere with neurotransmitter release by cleaving SNARE proteins. A key difference in their
transmitter in this specific sympathetic pathway. clinical manifestations is that:
A. Botulinum toxin causes spastic paralysis, while tetanus toxin causes flaccid paralysis.
44. A patient taking phenelzine (a non-selective, irreversible MAO inhibitor) consumes a meal rich in tyramine (e.g., aged cheese, red wine). This B. Botulinum toxin primarily affects peripheral cholinergic synapses (e.g., NMJ), causing flaccid paralysis, while tetanus
interaction is likely to precipitate:
toxin acts centrally on inhibitory
A. Severe hypotension and bradycardia. interneurons, causing spastic paralysis.
B. Bronchoconstriction and respiratory distress. C. Botulinum toxin enhances acetylcholine release, while tetanus toxin inhibits it.
C. A hypertensive crisis with severe headache and tachycardia. D. Botulinum toxin acts on adrenergic synapses, while tetanus toxin acts on cholinergic synapses.
D. Profound sedation and CNS depression. Answer: B) Explanation:
Answer: C) Explanation:
Correct (B):
Correct ©: Tyramine is an indirectly acting sympathomimetic amine found in certain foods. Normally, it is metabolized by MAO- Botulinum toxin acts peripherally, primarily at cholinergic nerve terminals (especially the neuromuscular junction),
A in the gut wall and liver. When MAO (especially MAO-A) is inhibited by a drug like phenelzine, ingested tyramine is absorbed blocking acetylcholine release and leading to flaccid paralysis. (ANS Intro Slide 54)
systemically, taken up into sympathetic nerve terminals, and displaces Tetanus toxin is taken up by motor neurons and transported retrogradely to the CNS (spinal cord). There, it acts primarily
large amounts of norepinephrine from storage vesicles. This massive release of on inhibitory interneurons (that release GABA or glycine), blocking the release of these inhibitory
neurotransmitters. This disinhibition of motor neurons leads to uncontrolled muscle contraction and spastic paralysis (e.g.,
norepinephrine causes potent vasoconstriction and cardiac stimulation, leading to a severe hypertensive crisis, often
“lockjaw”).
accompanied by headache and tachycardia. (ANS Intro Slide 67)
Incorrect (A): The paralysis types are reversed.
Incorrect (A, B, D): These are not characteristic of the tyramine-MAOI interaction.
Incorrect ©: Both inhibit neurotransmitter release by cleaving SNAREs (ACh for botulinum; GABA/glycine for tetanus).
45. The phenomenon of “receptor downregulation” in response to chronic agonist exposure primarily involves: Incorrect (D): Botulinum is primarily cholinergic. Tetanus affects GABAergic/glycinergic synapses in the CNS.
A. Increased synthesis of receptor proteins.
50. A patient being treated for hypertension with an alpha-1 selective blocker like prazosin experiences a significant drop in blood pressure upon
B. Enhanced coupling efficiency between the receptor and its G-protein. standing up from a seated position. This adverse effect is best termed:
 A. Reflex bradycardia. Incorrect (A & B): These describe ligand-gated ion channels (ionotropic receptors). Incorrect (D): While many presynaptic
B. Tachyphylaxis. autoreceptors are GPCRs, postsynaptic receptors for many neurotransmitters (e.g., muscarinic, adrenergic, most serotonin,
C. Orthostatic (postural) hypotension. dopamine) are also GPCRs.
D. Rebound hypertension.
Answer: C) Explanation: 56. Epinephrine reversal, where epinephrine causes hypotension in the presence of an alpha-blocker, occurs because:
A. Alpha-blockade enhances epinephrine’s affinity for beta-1 receptors, causing profound cardiac depression.
Correct ©: Orthostatic (or postural) hypotension is a fall in blood pressure that occurs upon assuming an upright posture B. Alpha-blockade unmasks epinephrine’s beta-2 receptor-mediated vasodilatory effects.
(standing up). Alpha-1 blockers cause C. Alpha-blockers directly stimulate beta-2 receptors, potentiating epinephrine’s vasodilatory action.
vasodilation by inhibiting sympathetic vasoconstrictor tone. This impairs the body’s ability to reflexively constrict blood vessels D. Alpha-blockade inhibits the reuptake of epinephrine, leading to excessive beta-2 stimulation.
in the lower extremities upon standing, leading to pooling of blood and a drop in BP. This is a common side effect, especially with Answer: B) Explanation:
initial doses (“first-dose phenomenon”). (Anti-Adrenergics Slide 120 - side effects implied)
Incorrect (A): Reflex bradycardia occurs in response to a rise in BP. Here, BP falls, which would trigger reflex tachycardia. Correct (B): Epinephrine has agonist activity at α1, α2, β1, and β2 receptors.
Incorrect (B): Tachyphylaxis is a rapid decrease in drug responsiveness. Incorrect (D): Rebound hypertension occurs upon Normally, α1-mediated vasoconstriction dominates its effect on blood pressure.
abrupt withdrawal of certain antihypertensives (e.g., clonidine). When α1 receptors are blocked (e.g., by prazosin or phenoxybenzamine), this
vasoconstrictor effect is abolished. Epinephrine’s β2-mediated vasodilatory effect (especially in skeletal muscle vascular beds)
51. The primary intracellular second messenger produced upon activation of Beta-1 and Beta-2 adrenoceptors is: then becomes unopposed, leading to a
A. Inositol trisphosphate (IP3). net decrease in peripheral resistance and a fall in blood pressure (hypotension). (Same principle as Q24 in first set)
B. Diacylglycerol (DAG). Incorrect (A): Alpha-blockade does not primarily enhance affinity for beta-1 receptors or cause cardiac depression directly.
C. Cyclic AMP (cAMP). Incorrect ©: Alpha-blockers antagonize alpha receptors; they do not stimulate beta-2 receptors.
D. Calcium ions (Ca2+). Answer: C) Explanation: Incorrect (D): Alpha-blockers do not primarily inhibit epinephrine reuptake (epinephrine is mainly cleared by uptake and
metabolism, not as reliant on NET as NE).
Correct ©: All Beta-adrenoceptor subtypes (β1, β2, β3) are coupled to Gs proteins. Activation of Gs stimulates the enzyme
adenylyl cyclase, which converts ATP to cyclic AMP (cAMP). cAMP then acts as a second messenger, typically by activating 57. A patient treated with an acetylcholinesterase inhibitor for myasthenia gravis develops excessive salivation, sweating, abdominal cramps, and
Protein Kinase A (PKA). (ANS Intro Slide 86, 87) bradycardia. These adverse effects are primarily due to excessive stimulation of:
Incorrect (A, B, D): IP3, DAG, and increased intracellular Ca2+ are typically associated with Gq-coupled receptors (e.g., Alpha- A. Nicotinic Nm receptors at the neuromuscular junction.
1, Muscarinic M1/M3/M5). B. Nicotinic Nn receptors in autonomic ganglia.
C. Muscarinic cholinoceptors on effector organs.
52. Which of the following autonomic nervous system structures is characterized by cholinergic preganglionic fibers and adrenergic D. Alpha and Beta adrenoceptors.
postganglionic fibers releasing norepinephrine? Answer: C) Explanation:
A. Parasympathetic pathway to the heart.
B. Sympathetic pathway to sweat glands. Correct ©: The symptoms described (salivation, sweating, abdominal cramps/GI hypermotility, bradycardia) are all classic
C. Somatic motor pathway to skeletal muscle. manifestations of excessive muscarinic receptor stimulation due to increased acetylcholine levels. AChE inhibitors increase ACh
D. Typical sympathetic pathway to most blood vessels. Answer: D) at both muscarinic and nicotinic sites, but these particular symptoms are mediated by muscarinic receptors on exocrine glands,
Explanation: GI smooth muscle, and the
heart. (Cholinomimetics Slide 109)
Correct (D): The typical sympathetic efferent pathway involves: Incorrect (A): Excessive Nm stimulation causes muscle fasciculations and weakness/paralysis.
Preganglionic neurons releasing acetylcholine (ACh) at the ganglion. Incorrect (B): Excessive Nn stimulation in ganglia would cause complex, widespread autonomic activation, not just these specific
Postganglionic neurons releasing norepinephrine (NE) at the neuroeffector junction (e.g., innervating smooth muscle of muscarinic symptoms.
most blood vessels to cause Incorrect (D): These are adrenergic receptors.
vasoconstriction). (ANS Intro Slide 15, 28, 29)
Incorrect (A): Parasympathetic pathway to heart: preganglionic ACh, postganglionic ACh. 58. The primary therapeutic advantage of using a selective Beta-1 adrenoceptor antagonist (e.g., metoprolol) over a non-selective beta-blocker (e.g.,
Incorrect (B): Sympathetic pathway to sweat glands: preganglionic ACh, postganglionic ACh. propranolol) in a patient with hypertension and concomitant asthma is:
Incorrect ©: Somatic pathway: single neuron releasing ACh. A. Greater reduction in blood pressure.
B. Longer duration of action.
53. A drug that causes mydriasis (pupil dilation), cycloplegia (paralysis of accommodation), dry mouth, and tachycardia is most likely acting as an C. Lower risk of precipitating bronchospasm.
antagonist at which type of receptor? D. More potent inhibition of renin release.
A. Nicotinic Nm receptors. Answer: C) Explanation:
B. Alpha-1 adrenoceptors.
C. Muscarinic cholinoceptors. Correct ©: Beta-2 adrenoceptors mediate bronchodilation. Non-selective beta- blockers like propranolol block both β1 (cardiac)
D. Beta-2 adrenoceptors. Answer: C) Explanation: and β2 (bronchial) receptors.
Blocking β2 receptors in an asthmatic patient can lead to bronchoconstriction and precipitate an asthma attack. Selective Beta-1
Correct ©: The constellation of symptoms described (mydriasis, cycloplegia, dry mouth, tachycardia, and others like urinary antagonists (“cardioselective,” like metoprolol or atenolol) preferentially block β1 receptors at therapeutic doses, thus having
retention, constipation, CNS effects) is characteristic of antimuscarinic (anticholinergic) drug effects, resulting from less effect on bronchial β2 receptors and a lower risk of causing
blockade of muscarinic acetylcholine receptors. Atropine is the prototype. (Anticholinergics Slide 113) bronchospasm in patients with reactive airway disease. (Anti-Adrenergics Slide 119) Incorrect (A): Both can be effective
Incorrect (A): Nicotinic Nm blockade causes muscle paralysis. antihypertensives.
Incorrect (B): Alpha-1 agonists cause mydriasis and vasoconstriction. Alpha-1 Incorrect (B): Duration of action varies between drugs, not solely by selectivity.
antagonists cause miosis (or prevent dilation) and vasodilation.
Incorrect (D): Beta-2 blockade causes bronchoconstriction. Beta-2 agonists cause bronchodilation/vasodilation. Incorrect (D): Renin release is β1-mediated, so both selective and non-selective agents will inhibit it.

54. The “axon reflex” or “sensory local effector” function, where sensory nerve activation leads to local release of peptides like Substance P and 59. The intracellular signaling pathway primarily associated with M1, M3, and M5 muscarinic acetylcholine receptors involves:
CGRP causing vasodilation and inflammation, is a characteristic of certain: A. Inhibition of adenylyl cyclase and decreased cAMP.
A. Sympathetic cholinergic neurons. B. Activation of adenylyl cyclase and increased cAMP.
B. Parasympathetic preganglionic neurons. C. Activation of phospholipase C, leading to IP3 and DAG formation and increased intracellular Ca2+.
C. Nonadrenergic, Noncholinergic (NANC) sensory neurons. D. Direct gating of an intrinsic ion channel within the receptor.
D. Somatic motor neurons. Answer: C) Explanation:
Answer: C) Explanation: Correct ©: M1, M3, and M5 muscarinic receptors are coupled to Gq/11 G-proteins.
Activation of Gq/11 stimulates phospholipase C (PLC), which then generates the second messengers inositol trisphosphate (IP3)
Correct ©: Some primary sensory afferent neurons (which are NANC, as they release peptides, not ACh or NE primarily) have
and diacylglycerol (DAG). IP3
peripheral branches that can release these peptides (Substance P, CGRP) locally upon stimulation. This “sensory- efferent” or
mobilizes intracellular calcium, and DAG activates protein kinase C. (ANS Intro Slide 73, 76)
axon reflex function contributes to neurogenic inflammation and
Incorrect (A): This describes Gi/Go-coupled receptors (e.g., M2, M4, Alpha-2). Incorrect (B): This describes Gs-coupled
vasodilation without necessarily involving central reflexes. (ANS Intro Slide 94) Incorrect (A, B, D): These other neuron types do
receptors (e.g., Beta-adrenoceptors). Incorrect (D): This describes ionotropic receptors (e.g., nicotinic receptors).
not primarily mediate this specific local peptide-releasing sensory-effector function.
60. Which of the following drugs acts by irreversibly inhibiting acetylcholinesterase, leading to prolonged accumulation of acetylcholine?
55. The primary role of G-protein coupled receptors (GPCRs) in synaptic transmission, compared to ligand-gated ion channels, is to: A. Neostigmine.
A. Mediate rapid, millisecond-timescale excitatory postsynaptic potentials.
B. Edrophonium.
B. Allow direct passage of ions across the postsynaptic membrane upon transmitter binding.
C. Atropine.
C. Initiate slower, longer-lasting modulatory changes in neuronal excitability and intracellular signaling cascades. D. Echothiophate (or Organophosphates like Parathion, Soman). Answer: D)
D. Act exclusively as autoreceptors on presynaptic terminals. Explanation:
Answer: C) Explanation:
Correct (D): Echothiophate is an organophosphate compound that forms a very
Correct ©: GPCRs (metabotropic receptors) do not form ion channels themselves. Their activation by neurotransmitters initiates stable, essentially irreversible (unless an oxime is given early) covalent bond with the active site of acetylcholinesterase. This
intracellular signaling cascades via leads to long-lasting inhibition of the
G-proteins and second messengers. These processes have a slower onset (seconds to minutes) and longer duration, leading to enzyme and prolonged accumulation of ACh. Other organophosphates (insecticides, nerve agents) act similarly. (Cholinomimetics
modulatory effects on ion channels, enzyme activity, or gene expression, rather than direct fast synaptic potentials. (ANS Intro Slide 105)
Slide 42, 45) Incorrect (A & B): Neostigmine and Edrophonium are reversible AChE inhibitors (carbamates and simple alcohol, respectively).
 Incorrect ©: Atropine is a muscarinic receptor antagonist, it does not inhibit AChE. sympathetic vasoconstrictor tone.
C. Blocking beta-1 adrenoceptors in the heart.
61. The process of “redistribution” is most clinically significant in terminating the initial CNS effects of which type of drug administered intravenously? D. Stimulating alpha-2 adrenoceptors in the CNS.
A. A highly water-soluble drug with a small volume of distribution. Answer: B) Explanation:
B. A highly lipid-soluble drug with a large ultimate volume of distribution. Correct (B): Ganglionic blockers antagonize nicotinic (Nn) receptors in all autonomic ganglia (sympathetic and
C. A drug that is rapidly metabolized by plasma esterases. parasympathetic). By blocking sympathetic
D. A drug that binds irreversibly to its CNS receptors. ganglia, they reduce the transmission of signals that maintain tonic vasoconstriction of blood vessels. This reduction in
Answer: B) Explanation: sympathetic vasoconstrictor tone leads to
Correct (B): Redistribution describes the phenomenon where a highly lipid-soluble drug, after rapid IV administration, initially vasodilation and a fall in blood pressure. They also block parasympathetic ganglia, leading to many side effects. (Anticholinergics
Slide 111)
distributes to well-perfused organs (like the brain, causing rapid onset of CNS effects). As plasma levels fall, the drug then
Incorrect (A): They don’t cause direct vasodilation; the vasodilation is indirect via reduced sympathetic tone.
rapidly leaves these organs and redistributes to less well-perfused but larger tissue compartments (like muscle and fat). This Incorrect ©: This describes beta-blockers.
movement out of the brain terminates the initial CNS effect, even though the drug has not yet been eliminated from the body. Incorrect (D): This describes centrally acting alpha-2 agonists like clonidine.
Thiopental is the classic example. (ANS Intro Slide 108)
Incorrect (A): Water-soluble drugs with small Vd tend to remain in the plasma/ECF and don’t redistribute extensively into 67. What is the physiological consequence of activating M2 muscarinic receptors in the sinoatrial (SA) node of the heart?
tissues like fat. A. Increased rate of spontaneous depolarization and tachycardia.
Incorrect ©: Rapid metabolism would terminate effects, but this is distinct from redistribution. B. Decreased rate of spontaneous depolarization, hyperpolarization, and bradycardia.
Incorrect (D): Irreversible binding would cause prolonged effects, not termination by redistribution. C. Increased force of atrial contraction.
D. Shortening of the action potential duration in ventricular myocytes.
62. The primary neurotransmitter mediating fast excitatory transmission at autonomic ganglia is: Answer: B) Explanation:
A. Norepinephrine acting on alpha-1 receptors.
B. Acetylcholine acting on nicotinic (Nn) receptors. Correct (B): M2 muscarinic receptors in the SA node are coupled to Gi proteins. Activation by acetylcholine (e.g., from vagal
C. Acetylcholine acting on muscarinic (M1) receptors. stimulation) inhibits adenylyl cyclase (decreasing cAMP) and, importantly, activates GIRK (G-protein coupled inwardly rectifying
D. Dopamine acting on D1 receptors. K+) channels. The opening of these K+ channels leads to K+ efflux, hyperpolarization of the SA node cells, and a slowing of the
Answer: B) Explanation: rate of spontaneous
diastolic depolarization, resulting in bradycardia (decreased heart rate). (ANS Intro Slide 74, 75)
Correct (B): Preganglionic neurons in both the sympathetic and parasympathetic divisions release acetylcholine (ACh) at the Incorrect (A): This describes sympathetic (Beta-1) stimulation. Incorrect ©: M2 activation decreases atrial
autonomic ganglia. This ACh acts on contractility.
Nicotinic (Nn type) cholinergic receptors on the postganglionic neurons, which are ligand-gated ion channels. Activation of Incorrect (D): While ACh can affect ventricular action potentials, its most prominent effect is on nodal tissue and atrial function.
these Nn receptors causes rapid The primary effect on SA node is
depolarization (an excitatory postsynaptic potential, EPSP) leading to fast slowing.
transmission of the signal to the postganglionic neuron. (ANS Intro Slide 5, 15, 41, 79)
Incorrect (A): Norepinephrine is released by postganglionic sympathetic neurons at effector organs. 68. The primary therapeutic use of ipratropium bromide, a quaternary ammonium antimuscarinic agent, is in the management of:
Incorrect ©: While M1 muscarinic receptors are also present in ganglia and contribute to a slow, modulatory EPSP, the fast A. Overactive bladder.
primary transmission is nicotinic. Incorrect (D): Dopamine can be a transmitter in some ganglionic interneurons or specific B. Motion sickness.
pathways but is not the primary fast excitatory transmitter in most autonomic ganglia. C. Peptic ulcer disease.
D. Bronchospastic disorders like COPD and asthma. Answer: D)
63. A patient is given a drug that causes miosis, increased salivation, bronchoconstriction, and bradycardia. These effects are blocked by atropine. The Explanation:
drug given is most likely a(n):
A. Nicotinic receptor agonist. Correct (D): Ipratropium is a non-selective muscarinic antagonist. As a quaternary amine, it is poorly absorbed systemically
B. Muscarinic receptor agonist. when inhaled. It is administered via inhalation to block M3 muscarinic receptors on bronchial smooth muscle, causing
C. Alpha-adrenoceptor agonist. bronchodilation, and to reduce mucus secretion. It is used primarily for COPD and sometimes for asthma. (Anticholinergics Slide
D. Beta-adrenoceptor agonist. 112)
Answer: B) Explanation: Incorrect (A): While antimuscarinics are used for OAB, ipratropium’s formulation and properties are optimized for inhalation,
not systemic effects on the bladder. Incorrect (B): Scopolamine (tertiary amine, crosses BBB) is used for motion sickness.
Correct (B): The symptoms described (miosis, salivation, bronchoconstriction,
bradycardia) are all characteristic effects of stimulating muscarinic acetylcholine receptors (parasympathomimetic effects). Incorrect ©: M1 selective antagonists (like pirenzepine, historically) or other drug classes are used for PUD.
Atropine is a competitive muscarinic receptor antagonist, so it would block these effects. Drugs like pilocarpine or 69. Which of the following is a characteristic effect of Alpha-2 adrenoceptor activation in the central nervous system?
bethanechol would produce this profile. (Cholinomimetics Slide 107) A. Increased release of norepinephrine from central noradrenergic neurons.
Incorrect (A): Nicotinic agonists primarily affect ganglia and the neuromuscular junction, leading to different effects (e.g., muscle B. Decreased sympathetic outflow from the brainstem vasomotor centers.
fasciculations, widespread autonomic activation). C. Vasodilation of cerebral blood vessels.
Incorrect (C & D): Adrenergic agonists would produce sympathomimetic effects (e.g., mydriasis, tachycardia, bronchodilation). D. Stimulation of the emetic center (chemoreceptor trigger zone).
Answer: B) Explanation:
64. Which of the following drugs is a selective Beta-2 adrenergic agonist primarily used for its bronchodilator effects in asthma?
A. Isoproterenol. Correct (B): Alpha-2 adrenoceptors are located in brainstem areas that regulate sympathetic outflow (e.g., NTS, rostral
B. Dobutamine. ventrolateral medulla). Activation of these
C. Albuterol (Salbutamol). central alpha-2 receptors (e.g., by clonidine) inhibits sympathetic neurons, leading to a decrease in sympathetic outflow to the
D. Phenylephrine. Answer: C) Explanation: periphery, resulting in reduced heart rate, cardiac output, and peripheral vascular resistance (antihypertensive effect). (ANS
Intro Slide 85)
Correct ©: Albuterol (Salbutamol) is a short-acting selective Beta-2 adrenergic agonist. Activation of Beta-2 receptors on Incorrect (A): Activation of presynaptic alpha-2 autoreceptors decreases NE release. Incorrect ©: Cerebral vasoconstriction or
bronchial smooth muscle leads to relaxation and bronchodilation, making it a first-line rescue medication for asthma. complex effects can occur; vasodilation is not a primary, general effect.
(Sympathomimetics Slide 117) Incorrect (D): Some alpha-2 agonists can cause sedation, but direct stimulation of the emetic center is not their characteristic CNS
Incorrect (A): Isoproterenol is a non-selective Beta (β1 and β2) agonist; its β1 effects cause significant tachycardia. effect.
Incorrect (B): Dobutamine is primarily a Beta-1 agonist used for cardiac stimulation.
Incorrect (D): Phenylephrine is an Alpha-1 agonist used as a decongestant/vasopressor. 70. The “cheese reaction,” a severe hypertensive crisis, can occur when patients taking non- selective MAO inhibitors ingest foods rich in:
A. Acetylcholine.
65. The “fight-or-flight” response is initiated by increased activity of the sympathetic nervous system and release of epinephrine from the adrenal B. Histamine.
medulla. Which receptor subtype is primarily responsible for increasing heart rate and contractility during this response? C. Tyramine.
A. Alpha-1 adrenoceptors. D. Serotonin. Answer: C) Explanation:
B. Alpha-2 adrenoceptors.
C. Beta-1 adrenoceptors. Correct ©: Tyramine is an indirectly acting sympathomimetic amine present in aged, fermented, or spoiled foods (e.g., aged
D. Beta-2 adrenoceptors. Answer: C) Explanation: cheeses, red wine, cured meats).
Normally, ingested tyramine is metabolized by MAO-A in the gut wall and liver. If a patient is taking a non-selective MAO
Correct ©: Beta-1 adrenoceptors are located predominantly in the heart (SA node, inhibitor (or an MAO-A inhibitor), this metabolic pathway is blocked. Absorbed tyramine then enters systemic circulation, is
AV node, myocardium). Stimulation of these receptors by norepinephrine (from sympathetic nerves) and epinephrine (from taken up into sympathetic nerve terminals, and displaces large amounts of
adrenal medulla) leads to increased norepinephrine, leading to a hypertensive crisis. (ANS Intro Slide 67)
heart rate (positive chronotropy), increased force of contraction (positive inotropy), and increased conduction velocity. (ANS Incorrect (A, B, D): While these are biogenic amines, the “cheese reaction” is
Intro Slide 86) specifically associated with tyramine due to its presence in food and its potent indirect sympathomimetic action when MAO is
Incorrect (A): Alpha-1 receptors primarily mediate vasoconstriction. Incorrect (B): Alpha-2 receptors are mainly inhibited.
inhibitory (presynaptic, CNS).
Incorrect (D): Beta-2 receptors mediate bronchodilation and vasodilation in certain beds. 71. The enzyme primarily responsible for the rapid inactivation of catecholamines within the cytoplasm of adrenergic nerve terminals (after reuptake
or before vesicular storage) is:
66. The primary mechanism by which ganglionic blocking drugs (e.g., trimethaphan) reduce blood pressure is by: A. Catechol-O-methyltransferase (COMT).
A. Direct vasodilation of peripheral arterioles. B. Monoamine oxidase (MAO).
B. Inhibiting neurotransmission through both sympathetic and parasympathetic autonomic ganglia, thereby reducing C. Tyrosine hydroxylase.
 D. Dopamine β-hydroxylase. 77. The primary mechanism by which varenicline aids in smoking cessation is:
Answer: B) Explanation: A. Irreversible inhibition of acetylcholinesterase in the CNS.
Correct (B): Monoamine oxidase (MAO) is located on the outer membrane of mitochondria within the cytoplasm of adrenergic B. Partial agonism at central alpha-4-beta-2 nicotinic acetylcholine receptors.
(and other monoaminergic) nerve terminals. Norepinephrine that is taken back up into the terminal by NET, or C. Complete blockade of all nicotinic receptors, preventing nicotine reward.
norepinephrine that is newly synthesized but not yet packaged into vesicles, is susceptible to degradation by MAO. (ANS Intro D. Enhancement of dopamine reuptake in the mesolimbic pathway.
Slide 62, 64, 65) Answer: B) (This requires knowledge beyond the provided slides but is a common ANS- related clinical drug.)
Incorrect (A): COMT primarily acts extraneuronally or on circulating catecholamines. It is largely absent from Explanation:
sympathetic nerve terminals. Incorrect ©: Tyrosine hydroxylase is a synthetic enzyme.
Correct (B): Varenicline is a partial agonist at α4β2 nicotinic acetylcholine receptors in the brain. These receptors are thought to
Incorrect (D): Dopamine β-hydroxylase is a synthetic enzyme located within synaptic vesicles.
be critical for the reinforcing (rewarding) effects of nicotine. As a partial agonist, varenicline:
72. A patient is administered an IV bolus of a highly lipid-soluble drug that acts on the CNS. The initial rapid offset of the drug’s CNS effect, despite a Provides some nicotinic stimulation, which can reduce nicotine withdrawal symptoms and cravings.
relatively long elimination half- life, is most likely due to: Simultaneously, by occupying the receptor, it blocks nicotine from binding and exerting its full agonist effect if the person
A. Rapid metabolic inactivation by CYP450 enzymes in the brain. smokes, thereby reducing the
B. Redistribution of the drug from the CNS to other body tissues (e.g., muscle, fat). perceived reward from smoking.
C. Efficient active transport of the drug out of the CNS by P-glycoprotein. Incorrect (A): Varenicline does not inhibit AChE. Incorrect ©: It’s a partial agonist, not a complete
D. Saturation of CNS receptors leading to acute tachyphylaxis. blocker.
Answer: B) Explanation: Incorrect (D): It indirectly affects dopamine release by modulating nicotinic receptors, but doesn’t directly enhance dopamine
reuptake.
Correct (B): This describes the phenomenon of redistribution. Highly lipid-soluble drugs rapidly enter the well-perfused brain,
causing a quick onset of CNS effects. 78. A patient experiences dry mouth, blurred vision, tachycardia, and difficulty urinating after starting a new medication. These symptoms are
However, as the drug concentration in the plasma falls (due to distribution to other tissues, not necessarily elimination), the most consistent with blockade of which neurotransmitter system?
drug rapidly leaves the brain and moves into larger, less well-perfused tissue compartments like muscle and adipose tissue. This A. Adrenergic beta-1 receptors.
movement out of the brain terminates the initial CNS effect, even if the drug is slowly eliminated from the body overall. B. Adrenergic alpha-1 receptors.
Thiopental is a classic example. (ANS Intro Slide 108) C. Dopaminergic D2 receptors.
Incorrect (A): While some CNS metabolism occurs, redistribution is usually faster for these types of drugs. D. Cholinergic muscarinic receptors. Answer: D)
Explanation:
Incorrect ©: P-glycoprotein contributes to limiting CNS entry, but redistribution is key for offset of effect for highly lipid-soluble
IV bolus drugs. Correct (D): This constellation of symptoms (dry mouth, blurred vision/cycloplegia, tachycardia, urinary retention) is the
Incorrect (D): Tachyphylaxis is a rapid decrease in receptor responsiveness, not directly related to drug disposition. hallmark of antimuscarinic (anticholinergic) drug effects, caused by blockade of acetylcholine’s action at muscarinic receptors
throughout the body. (Anticholinergics Slide 113) Incorrect (A): Beta-1 blockade causes
73. Which of the following neurotransmitters primarily acts on G-protein coupled receptors to produce its effects, rather than directly gating an ion
channel? bradycardia.
A. Acetylcholine at the neuromuscular junction. Incorrect (B): Alpha-1 blockade primarily causes vasodilation/hypotension. Incorrect ©: D2 blockade is associated with
B. GABA acting on GABA-A receptors. antipsychotic effects and potential extrapyramidal symptoms.
C. Glutamate acting on AMPA receptors.
79. The adrenal medulla is functionally most analogous to:
D. Norepinephrine acting on alpha and beta adrenoceptors. Answer: D)
A. A parasympathetic ganglion.
Explanation:
B. A sympathetic ganglion where postganglionic neurons have become endocrine cells.
Correct (D): All known alpha and beta adrenoceptors, which are the receptors for norepinephrine (and epinephrine), are G- C. A somatic motor neuron.
protein coupled receptors (GPCRs). They signal via second messenger systems. (ANS Intro Slide 82) vasoconstrictor effects of alpha-1 agonism coupled with the expected baroreceptor reflex response on heart rate.
Incorrect (A): ACh at the NMJ acts on Nicotinic (Nm) receptors, which are ligand- gated ion channels.
Incorrect (B): GABA-A receptors are ligand-gated chloride channels. (GABA-B receptors are GPCRs, but GABA-A is the more
common “fast” inhibitory receptor).
Incorrect ©: AMPA receptors (and NMDA, Kainate) for glutamate are ligand-gated cation channels.

74. The physiological response to stimulation of Beta-2 adrenoceptors includes all of the following EXCEPT:
A. Bronchodilation.
B. Vasodilation in skeletal muscle vascular beds.
C. Uterine smooth muscle relaxation (tocolysis).
D. Increased heart rate and contractility. Answer: D)
Explanation:

Incorrect (D is the exception): Increased heart rate and contractility are primarily mediated by Beta-1 adrenoceptors located in the heart.
(ANS Intro Slide 86)
Correct (A, B, C): Bronchodilation, vasodilation of blood vessels supplying skeletal muscle, and uterine relaxation are all
characteristic effects of Beta-2 adrenoceptor stimulation.

75. A drug that selectively blocks M1 muscarinic acetylcholine receptors would be expected to primarily interfere with:
A. Acetylcholine-induced slowing of the heart rate.
B. Acetylcholine-induced contraction of bronchial smooth muscle.
C. Acetylcholine-mediated slow excitatory postsynaptic potentials (EPSPs) in autonomic ganglia and CNS cognitive
functions.
D. Acetylcholine-induced skeletal muscle contraction at the neuromuscular junction.
Answer: C) Explanation:

Correct ©: M1 muscarinic receptors are prominently located in autonomic ganglia where they mediate slow EPSPs, and in the
CNS where they are involved in cognitive processes (e.g., memory, learning). A selective M1 antagonist (like pirenzepine,
though its selectivity is relative) would interfere with these functions. (ANS Intro Slide 73, 77, 78)
Incorrect (A): Cardiac slowing is primarily mediated by M2 receptors.
Incorrect (B): Bronchial smooth muscle contraction is primarily mediated by M3 receptors.
Incorrect (D): Skeletal muscle contraction is mediated by Nicotinic Nm receptors.

76. The therapeutic index (TI) of a drug, often calculated as TD50/ED50, provides a measure of the drug’s:
A. Potency.
B. Maximal efficacy.
C. Relative safety margin.
D. Rate of elimination. Answer: C) Explanation:

Correct ©: The Therapeutic Index (TI) is a quantitative measure of a drug’s relative safety. It compares the dose (or
concentration) that produces a desired therapeutic effect in 50% of the population (ED50) to the dose that produces a specific
toxic effect in 50% of the population (TD50). A larger TI indicates a wider margin between
effective and toxic doses, suggesting greater safety. (Pharmacodynamics Slides 214, 216)
Incorrect (A): Potency is related to ED50 (dose for effect).
Incorrect (B): Maximal efficacy (Emax) is the largest effect a drug can produce. Incorrect (D): Rate of elimination is related to
clearance and half-life.